Keloids are an example of abnormal scars that grow beyond the boundaries of the original skin injury site, and have the appearance of a raised amorphous growth, frequently associated with pruritus and pain. Histologically, keloids can be distinguished by the randomly organized collagen fibers in a dense connective tissue matrix, whereas in normal scars the collagen bundles are generally parallel to the skin surface. The most common keloid sites in the head and neck are the earlobes, mandibular border and posterior neck.
Abnormal scars also include spread scars and hypertrophic scars. Spread scars occur when a wound is not properly closed or secondary to original wound breakdown. Hypertrophic scars occur with a similar histology to keloid scars, but usually occur when the wound is under stress.
The pathophysiology of keloids and other abnormal scars is not well understood. A leading theory is that fibroblasts and myofibroblasts are responsible for depositing a dense extracellular matrix of collagen and glycosaminoglycans. Elevated fibronectin production has been reported by keloidal fibroblasts. Other theories include: an allergic immunoglobulin E (IgE)-mediated response, leading to a decreased percentage of mature cross-linked collagen and an increased fraction of soluble collagen; a deficiency in melanocyte-stimulating hormone (MSH) metabolism or an excess of MSH, noting that increases in MSH and subsequent keloid formation are associated with pregnancy and puberty; microvascular occlusion and subsequent hypoxia; elevated interleukin-6 (IL-6) expression; and insulinlike growth factor-1 (IGF-1) and IGF-1 receptor axis in the invasive activity of keloids.
Surgical, non-surgical and combined modality treatments have been used or proposed, with limited success; e.g. recurrence rates of 50-80% are accepted. One of the most common therapies known is cold-knife excision followed by intralesional steroid injection, usually 2-3 weeks postoperatively with a repeat injection in 3-4 weeks to delay wound healing and increase the likelihood of wound dehiscence. Corticosteroids work by inhibiting fibroblast growth and promoting collagen degradation. Triamcinolone suspension at 10 mg/mL is commonly used, although dexamethasone and cortisone have also been used. Higher triamcinolone concentrations to 40 mg/mL have been used for dense, recalcitrant keloids, but the risk of depigmentation and dermal atrophy are greater. Still, reported recurrence rates low.
More aggressive keloid treatment therapies have included radiation therapy, without statistical significance but a slightly lower recurrence rate. However, aggressive therapies such as radiation for treatment of benign conditions have potential disadvantages such as, for example, thyroid or salivary gland neoplasia which have a latency of 15-20 years.